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Prolactin Enhances CCAAT Enhancer-Binding Protein-ß (C/EBPß) and Peroxisome Proliferator-Activated Receptor (PPAR) Messenger RNA Expression and Stimulates Adipogenic Conversion of NIH-3T3 Cells

Helix Research Institute (R.N.-W., Y.M., M.-a.M., H.W.) Chiba, 292-0812, Japan
The First Department of Internal Medicine (Y.F.) Osaka University Medical School Osaka, 565 Japan

Extracellular stimuli trigger adipocyte differentiation by inducing the complex cascades of transcription. Transcription factors CCAAT enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor (PPAR) play crucial roles in this process. Although ectopic expression of these factors in NIH-3T3 cells, a multipotential mesenchymal stem cell line, results in adipogenic conversion, little is known as to hormonal factors that regulate adipogenesis in these cells. In this report we demonstrate that PRL, a lactogenic hormone, enhances C/EBPß and PPAR mRNA expression and augments adipogenic conversion of NIH-3T3 cells. Moreover, we show that ectopic expression of the PRL receptor in NIH-3T3 cells results in efficient adipocyte conversion when stimulated with PRL and a PPAR ligand, as evidenced by expression of the adipocyte differentiation-specific genes as well as the presence of fat-laden cells. We further demonstrate that signal transducer and activator of transcription 5 (Stat5), a PRL signal transducer, activates aP2 promoter in a PRL-dependent manner. These results suggest that PRL acts as an adipogenesis-enhancing hormone in NIH-3T3 cells.

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